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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During a 5-year period from 1979 to 1983 all patients in Denmark with metastatic non-seminomatous and extragonadal germ cell cancer were treated with 6 cycles of cisplatin, vinblastine, and bleomycin (PVB). Thirty-nine patients referred to the Finsen Institute accepted a follow-up examination of side-effects 3.5-9 years after chemotherapy. Renal toxicity consisted of an irreversible decrease in glomerular filtration rate (GFR) in 47% of the patients, while the decrease in GFR was fully reversible in 23%. Significant pulmonary toxicity was observed in smokers and consisted of an irreversible decrease in carbon monoxide diffusion capacity to median 72% of the predicted value. Neurotoxicity was the most pronounced long-term side-effect. Nearly all patients had a peripheral sensory neuropathy probably caused by axonal degeneration. A central conduction defect was observed in 88% of the patients by measuring auditory brain-stem potentials. Irreversible high-frequency hearing loss was induced in 39% of the patients. Parasympathetic nerve dysfunction was found in 36% of the examined patients, including 2 patients with impotence. Half of the patients revealed Raynaud's phenomenon (RP), and the mechanism underlying this side-effect was found to be hyperreactivity of the central sympathetic nervous system. Vascular toxicity was found only in terminal arterioles and was not responsible for RP. PVB treatment caused low sperm counts and a subclinical Leydig cell dysfunction in the majority of patients. Azoospermia was observed in 27% of the patients. Six patients had hypertension and this was not related to renal impairment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Late-effects after treatment for germ-cell cancer with cisplatin, vinblastine, and bleomycin. 138 50

Among many metabolic disorders, porphyrias and Fabry disease are known to affect autonomic nervous system. In patients with acute intermittent porphyria, hereditary coproporphyria, and variegate porphyria, autonomic symptoms such as abdominal pain, vomiting, hypertension and tachycardia are among the most prominent clinical manifestations. Fabry disease is clinically characterized by severe limb pain, hypohidrosis, angiokeratomas and various autonomic symptoms. In both porphyrias and Fabry disease, pathological changes in the central and peripheral autonomic nervous system have been documented. In porphyrias, a loss of myelinated fibers, axonal degeneration, and segmental demyelination in peripheral autonomic nerves as well as chromatolysis of several brain stem nuclei have been found. In Fabry disease, abnormal amount of the substrates of alpha-galactosidase, i.e. ceramide di- and trihexoside, are found to be accumulated in the central and peripheral autonomic nerves.
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PMID:[Autonomic dysfunction in metabolic diseases]. 161 65

Pain related to fibromyalgia may consist of a complex interaction of nociceptive, neuropathic, dysregulatory central nervous system and psychosomatic mechanisms. Nociceptor pain is based on the excitation of nervous sensors specialized to signal potentially harmful stimuli, i.e., the nociceptors. Metabolic deficiencies in muscle and neurogenic inflammation induced by the release of substance P and other neuropeptides from the peripheral nerve endings may result in chemical sensitization of nociceptors and an ensuing hyperalgesia particularly present in tender points. Neuropathic pain is due to pathological mechanisms within nerve cells and fibers in the peripheral and central nervous system. Pathophysiology may be related to compression (such as in the carpal tunnel syndrome or a vertebral disk herniation) or regeneration of nerves, resulting in ectopic impulse discharges and disturbances of axonal transport. The ensuing neuronal hyperexcitability and trophic changes induced by a disturbed axonal transport system may be major factors of pain in fibromyalgia. Dysregulatory pain denotes pain maintained by dysfunction of efferent control loops. Thus, if spinal motoneuron output results in excessive tension of postural muscle, nociceptors in muscles, tendons and joints might become more excited. Persistent abnormal spinal reflex transmission due to, e.g., peripheral trauma or inappropriate postural habits may result in a vicious circle between muscle hypertension and pain. Similarly, a defective sympathetic control may result in disturbed microcirculation and nociceptor excitation (e.g., in sympathetic algodystrophy). Many symptoms of pain in fibromyalgia (trigger points, pain referral, pain associated with muscle spasm or neurogenic joint immobilization) can be attributed to abnormal control mechanisms in a complex cybernetic system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiological mechanisms of fibromyalgia. 181 May 27

To better understand and treat painful conditions, one needs to identify the cause, discover the source, and develop knowledge of peripheral and central pain transmission; headaches are no exception. The development of appropriate animal models is important. Accordingly, we have reviewed the anatomy, neurochemistry, electrophysiology, and pharmacology of the trigeminovascular system in experimental animals and emphasized whenever possible the relevance of this final common pathway to migraine, cluster, and other headache syndromes in humans. For example, based on recent anatomic dissections, the pericarotid cavernous sinus plexus was suggested as an important focus to investigate cluster headache pathophysiology. This plexus is an anatomic point of convergence for the nerves giving rise to the signs of sympathetic and parasympathetic activity and sensory symptoms that develop in cluster patients. As in other nociceptive systems, trigeminovascular axons assume at least two important roles. One concerns the transmission of nociceptive information. Electrophysiologic evidence supports the trigeminal nucleus caudalis as an important site for the convergence of visceral (vessel) and somatic (forehead) inputs to mediate the referral of vascular pain to superficial tissues. A second important role concerns the initiation of local increases in blood flow and enhanced protein permeability (sterile inflammation) via the axonal release of vasoactive neuropeptides. Plasma extravasation develops within the dura mater following trigeminal stimulation. Extravasation can be blocked by the administration of ergot alkaloids or sumatriptan, a new serotonin-like agonist, and a prejunctional (neuronal) mechanism of action for these drugs (such as blockade of release) was suggested based on experimental evidence. Whether vasoconstriction also relates to the therapeutic efficacy remains to be determined. As in other organ systems, real or threatened tissue injury provides an important stimulus for depolarizing sensory fibers. The stimulus may come from external conditions such as reduced blood flow or hypoglycemia. The brain may also possess intrinsic neuronal mechanisms by which nociceptors may be synthesized (e.g., glutamate-induced neurotoxicity, seizures). Molecules of relevance include bradykinin, prostaglandins, leukotrienes, and potassium. Experimental evidence was presented demonstrating that the trigeminal nerve mediates hyperemia within cortical gray matter by axon-reflex like mechanisms. An important role for this nerve was established during the hyperemic period of recirculation after ischemia or during severe hypertension above the limits of autoregulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Basic mechanisms in vascular headache. 217 82

The relationship between the sympathetic nervous system and vascular smooth muscle has been assessed in adult and juvenile spontaneously hypertensive rats (SHR) and compared with age-matched Wistar-Kyoto rats (WKY) using ultrastructural and light microscopic morphometric analysis of the caudal artery. The absolute volume of smooth muscle in the caudal artery of adult SHR (14-19) months was 169% greater than that in WKY vessels. As well, the axonal volume was 89% greater than that in the WKY. There was also a 51% increase in the number of vesicles per volume of varicosity in SHR compared to WKY. At 3 weeks of age the volume of both smooth muscle and axons within the caudal artery of SHR and WKY was not significantly different. However, there was a significantly greater number of vesicles (25%) per unit volume of varicosity in the SHR compared to the WKY. Thus, in the caudal artery there appears to be a relationship between smooth muscle cell volume and axonal volume. An increase in arterial smooth muscle volume (whether it be due to growth or hypertrophy) is accompanied by an increase in axonal volume, or vice versa. The significant increase in the number of vesicles per unit volume of varicosity in the SHR, compared to the WKY reported here, is consistent with other published data indicating an increased availability or turnover of transmitter in these animals. Since the blood pressures of the SHR and WKY are similar at 3 weeks, the apparent increase in sympathetic nerve activity observed suggests that this may be an initiating factor in the development of high blood pressure in SHR.
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PMID:Relationship between the sympathetic nervous system and vascular smooth muscle: a morphometric study of adult and juvenile spontaneously hypertensive rat/Wistar-Kyoto rat caudal artery. 236 32

Long-term neuropsychological recovery of 24 severe head-injured patients was examined and correlated with acute measurements of intracranial pressure (ICP) and diffuse computed tomographic (CT) lesions. Intracranial hypertension (ICP greater than or equal to 20 mm Hg) was present acutely in 12 patients and absent in 12 patients. CT diagnoses of diffuse swelling (DS) was present in 12 patients, and diffuse axonal injury (DAI) in 12 patients. During chronic recovery, neuropsychological dysfunctioning was found in all cases. Patients with acute ICP elevations showed more intellectual and memory losses than those without acute ICP elevations. No neuropsychological differences were found between patients with DS and DAI injuries. The findings suggest secondary brain insults caused by intracranial hypertension may be more disruptive to long-term neuropsychological functioning than diffuse lesion type.
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PMID:Relation between intracranial pressure, computed tomographic lesion, and neuropsychological outcome. 239 21

We previously showed that specific angiotensin II (Ang II) binding sites are present in the canine nodose ganglion and peripheral vagus nerve, and that unilateral removal of the nodose ganglion results in loss of binding in the ipsilateral nucleus tractus solitarii and the dorsal motor nucleus of the vagus. An association of Ang II binding sites with both afferent and efferent vagal fibers is consistent with actions of the peptide on cardiac vagal tone and the baroreceptor reflex. To investigate possible transport of Ang II binding sites, quantitative in vitro receptor autoradiography was used to visualize binding after double ligation of the peripheral process of the cervical vagus nerve. One ligature was tied 0.2 to 0.5 cm distal to the nodose ganglion; the second ligature was tied on the same nerve 1.0 to 1.5 cm from the nodose ganglion. Twenty-four hours later, high-affinity Ang II binding sites (Ka = 0.46 +/- 0.08 nM) accumulated at the first ligature (the side nearest the nodose ganglion), indicating anterograde transport. Since accumulations of similar affinity sites were seen distal to the second ligature, retrograde transport of binding sites also occurred. These data reveal the existence of a mechanism for the bidirectional axonal transport of Ang II binding sites in the cervical portion of the vagus nerve.
Hypertension 1988 Feb
PMID:Bidirectional transport of angiotensin II binding sites in the vagus nerve. 245 65

A consecutive series of 41 patients aged less than 16 and admitted to the Department of Neurosurgery of the University of Milan in the period 1977-1978 following serious cranioencephalic trauma with Glasgow Coma Score (GCS) less than or equal to 7, duration of coma longer than 24 h and CT picture of diffuse lesion has been examined. These patients account for 5% of the paediatric cranial traumas observed in the same period and 66% of those in a state of coma. The CT picture made it possible to split patients into 3 groups: a) those without visible cerebral lesions and with subarachnoid and cisternal spaces present; b) those with small hyperdense lesions due to intraparenchymal or median/paramedian subcortical shearing lesions; c) those with marked constriction or absence of the 3rd ventricle and of the perimesencephalic cisterns. The first two pictures (a, b) were considered to be the expression of diffuse axonal damage, the last (c) of diffuse cerebral swelling. Intracranial pressure was monitored in about 50% of patients. The overall outcome of the series was favourable in more than 68% of cases with total mortality of 26.8%. Analysis of individual tomographic categories, however, showed that whereas the group of patients with diffuse axonal lesion presented nil mortality, those with diffuse cerebral swelling had 52% mortality owing to the onset of refractory intracranial hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diffuse traumatic cerebral injuries in children]. 261 90

The association of acute subdural hematoma (SDH) and diffuse axonal injury has received little attention in the literature. The authors report the clinicopathological findings in six patients who died of severe head injury in whom computerized tomography revealed acute SDH as the predominant lesion. All patients were injured in road traffic accidents and lost consciousness on impact. The mean total contusion index was 17.4 and sever contusions were seen in only two cases. All patients presented histological criteria of intracranial hypertension (pressure necrosis focus in one or both parahippocampal gyri). Hypoxic brain damage was evident in the postmortem examination of three patients. In three cases, macroscopic hematic lesions were observed in the corpus callosum. All patients had widespread axonal retraction balls disseminated in the white brain matter. Three patients who survived for more than 11 days had microglial clusters. In some patients with a head injury, acute SDH may be only an epiphenomenon of a primary impact lesion of variable severity: that is, a diffuse axonal injury. In these cases, the final outcome is fundamentally dependent on the severity of the subjacent diffuse axonal injury.
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PMID:Acute subdural hematoma and diffuse axonal injury after severe head trauma. 337 84

Current-generation CT scanners enable the visualization in vivo of structures and substructures that were previously unobservable. Certainly the orbit and optic nerve/sheath complex have demonstrated a great number of pathologic and normal anatomic variations. It has been found in patients with elevated intracranial pressure that what was previously thought to be simple papilledema in fact masks a surprisingly large component of optic papilla protrusion. There may be a variable amount of increased intercellular/axonal fluid within the optic disk in patients with increased intracranial pressure; however, a significant factor in the "swollen disk" is the simple transmission of pressure along the optic nerve sheath to the papilla, causing it to bulge. Further investigations with dynamic CT reveal that there is decreased perfusion of the optic disk in the active phase of severe increased intracranial pressure in patients with papilledema and/or protrusion as compared with normal control subjects. This depressed flow pattern seems to originate subacutely and appears to resolve in certain patients after normalization of the elevated pressure. These findings apparently indicate that clinical intervention in cases of intracranial hypertension to restore the hemodynamic status of the optic disk would be timely, and thereby avert irreversible damage. This suggests and supports the theory that increased intracranial pressure may lead to rapid vision loss by the mechanical mechanism of pressure projected directly to the junction of the optic nerve and optic nerve head, leading to decreased perfusion, ischemia, axonal flow stasis, and resultant optic nerve atrophy.
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PMID:"Papilledema": neuroradiologic evaluation of optic disk protrusion with dynamic orbital CT. 349 33


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